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Research on the Mineral Selenium

The following articles are presented as a reflection for the use of ionic minerals selenium as a dietary supplement and nutritional supplement. You will find more on selenium here. You can also purchase this diet supplement below.


Chemoprevention of colorectal tumors: role of lactulose
and of other agents.

Ponz de Leon M; Roncucci L
Dept. of Internal Medicine, University of Modena, Italy.
Scand J Gastroenterol Suppl (NORWAY) 1997, 222 p72-5

Chemoprevention can be defined as an attempt at cancer control in which the occurrence of the disease is prevented by the administration of one (or more) chemical compounds. Main problems in chemoprevention studies are the choice of a suitable drug, the choice of an appropriate intermediate or definitive end point, and the definition of the population which should be investigated. Main classes of chemopreventive agents include vitamins, non-steroid anti-inflammatory drugs, minerals such as calcium or selenium, and other antioxidants such as N-acetylcysteine. Chemoprevention is particularly appealing in colorectal cancer, either because these lesions develop through a multistep process, or owing to the concept of "field carcinogenesis'. Between 1985 and 1990 we carried out a controlled study in which antioxidant vitamins or lactulose were used in an attempt to prevent the recurrence of colorectal polyps after their endoscopic removal. Among the 209 patients who could be evaluated, polyps recurred in 5.7% of the individuals who were given vitamins (A, C and E), 14.7% of patients given lactulose and 35.9% of untreated controls (chi 2 = 17.1, P <0.001). The study suggested that either antioxidant vitamins or lactulose could be effective in reducing the recurrence rate of adenomatous polyps. In a subsequent on-going study, lower doses of the same vitamins were tested versus N-acetylcysteine (60a 40% reduction of the recurrence of polyps versus controls) in individuals given N-acetylcysteine, while the effect of lower doses of vitamins was less appreciable. Definitive results of the study should be available by the end of 1998.

Biochemical basis of selenomethionine-mediated inhibition during 2-acetylaminofluorene-induced hepatocarcinogenesis in the rat.

Mukherjee B; Sarkar A; Chatterjee M
Department of Pharmaceutical Technology, Jadavpur University, Calcutta, India.
Eur J Cancer Prev (ENGLAND) Dec 1996, 5 (6) p455-63

Supplementation of selenium in the form of selenomethionine (8 ppm) in drinking water daily has been found to be highly effective in reducing cancer incidence in male Sprague-Dawley rats fed 2-acetylaminofluorine (2-AAF) (0.05%) in the basal diet daily for 16 weeks. Selenomethionine treatment before initiation, during initiation or during the selection/promotion phases of hepatocarcinogenesis has been found to be effective in elevating hepatic microsomal cytochrome b5, cytochrome P-450 contents, triphosphopyridine nucleotide-cytochrome c-reductase and cytosolic aryl hydrocarbon hydroxylase activities to a statistically significant level measured either in the hyperplastic nodules or in the non-nodular surrounding liver parenchyma compared with 2-AAF control rats. Moreover, selenomethionine treatment throughout the study also decreased the cytosolic 1-chloro-2,4-dinitrobenzene conjugated glutathione-S-transferase and microsomal UDP-glucuronyl transferase activities to a significant level when compared with 2-AAF control rats. Furthermore, direct correlations between hyperplastic nodules and non-nodular liver areas were observed with the hepatic selenium content and also with the rates and patterns of hepatic drug metabolism. Selenomethionine was also found to protect and improve the histopathological indices without any toe haematoxylin and eosin staining. Our results establish the fact that selenium is particularly protective in limiting the action of 2-AAF during the initiation phase of hepatocarcinogenesis.

Selenium: a quest for better understanding.

Badmaev V; Majeed M; Passwater RA
Sabinsa Corporation, Piscataway, NJ, USA.
Altern Ther Health Med (UNITED STATES) Jul 1996, 2 (4) p59-62, 65-7

Selenium is an essential trace element in nutrition for the prevention of disease in humans. Epidemiological studies indicate an association between low nutritional selenium status and increased risks of cardiomyopathy, cardiovascular disease, and carcinogenesis in various sites of the body. The role of selenium supplementation in the prevention and treatment of AIDS-related pathology has been considered. Selenoproteins discovered in mammalian cells may account for the essentiality of selenium in the body's antioxidant defense; thyroid hormone function; immune system function, particularly the cellular immunity; formation of sperm; and functioning of the prostate gland. The seleno-organic compounds, primarily L-(+)-selenomethionine, generally are recognized as safe and effective forms of selenium supplementation. The nutritionally recommended dose of elemental selenium is estimated at 50 to 200 mg per day. There is, however, increased discussion of a pharmacological dose of selenium, significantly higher than the nutritional dose of the microelement, to treat active conditions. One way of increasing the tissue levels of selenium is to combine its ingestible form with a nutrientilability enhancing compound. (87 Refs.)

Selenium as a risk factor for cardiovascular diseases.

Neve J
Universite Libre de Bruxelles, Institut de Pharmacie, Belgium.6277
J Cardiovasc Risk (ENGLAND) Feb 1996, 3 (1) p42-7

Selenium is a powerful antioxidant regulating the activity of the glutathione peroxidase enzymes, which catalyse the detoxification of hydrogen peroxide and organic hydroperoxides. Selenium deficiency has been implicated in the aetiopathogeny of Keshan disease, an endemic cardiomyopathy observed in China, and in other cases of congestive cardiomyopathy in subjects on artificial nutrition. However, the evidence from case-control and prospective studies for an association between low selenium status and cardiovascular diseases remains controversial. Mechanisms whereby selenium protects against such diseases include increased resistance of low-density lipoproteins against oxidative modification, modulation of prostaglandin synthesis and platelet aggregation, and protection against toxic heavy metals. The therapeutic benefit of selenium administration in the prevention and treatment of cardiovascular diseases still remains insufficiently documented.

[Selenium, glutathione peroxidase, peroxides and platelet functions]

Vitoux D; Chappuis P; Arnaud J; Bost M; Accominotti M; Roussel AM
Laboratoire central de biochimie, hopital Lariboisiere, Paris, France.
Ann Biol Clin (Paris) (FRANCE) 1996, 54 (5) p181-7

In the last five years, there has been a renewal of interest in the protective role of selenium in vascular disorders, inspired by experimental evidence that this trace element could modulate leukotriene and prostaglandin synthesis in both endothelial cells and platelets. In people living in low-selenium areas, a relationship has been established between a decrease in plasma selenium and an increase in the risk of coronary disease, atherosclerosis, platelet hyperaggregability and synthesis of proaggregant and proinflammatory compounds like thromboxane A2 and leukotrienes. Selenium, as an essential part of glutathione peroxidase, takes part in the reduction of hydrogen peroxides and lipid peroxides. The concentration of these peroxides, in turn, regulates the activities of cyclooxygenase and lipooxygenase pathways, ultimately influencing the production of eicosanoids and modulating the balance between a proaggregatory and antiaggregatory state. Recent evidence shows that selenium, via its action on glutathione peroxidase activity, may be primarily responsible for the regulation of the endogenous hydroperoxide level. In human platelets, the activity of glutathione peroxidase is particularly high and is very sensitive to the requirement of selenium. This sensitivity could explain why platelets of selenium-deficient subjects show increased aggregation, thromboxane B2 production and synthesis of the lipoxygenase-derived compounds. In these deficient subjects, selenium administration increases platelet glutathione peroxidase activity and inhibits platelet hyperaggregation and leukotriene synthesis. These results support the hypothesis that selenium supplementation has a positive effect on platelet aggregation in selenium-deficient subjects. In France, more than 10% of the population is selenium-deficient and long-term supplementation with low doses of selenium could have a beneficial effect on the prevention of both thrombosis and coronary heart disease in these subjects. (35 Refs.)

Deliberations and evaluations of the approaches, endpoints and paradigms for selenium and iodine dietary recommendations.

Levander OA; Whanger PD
U.S. Department of Agriculture, Agricultural Research Service, Beltsville Human Nutrition Research Center, MD 20705, USA.
J Nutr (UNITED STATES) Sep 1996, 126 (9 Suppl) p2427S-2434S

Information is presented regarding the approaches that have been used to establish dietary recommendations for selenium and iodine. In the case of selenium, activity of the selenoenzyme glutathione peroxidase has served as a convenient biochemical endpoint for judging nutritional status. However, there are differences of opinion among various nutritionists as to whether full expression of this enzymatic activity is required for adequate nutriture, thereby resulting in differences in dietary recommendations. Endpoints for assessing selenium overexposure are much less satisfactory, but toxicological standards for selenium have nevertheless been established. Thus far, no nutritionists have attempted to shift the paradigm for determining dietary selenium recommendations away from prevention of deficiency disease to prevention of chronic degenerative disease (e.g., cancer). In the case of iodine, urinary excretion of the element is the most widely used endpoint for judging nutritional status. Numerous epidemiological surveys have been conducted to determine the level of urinary iodine excretion that is consistent with prevention of goiter, the most common endpoint of iodine deficiency. Because dietary iodine is essentially quantitatively excreted in the urine, determination of the latter in goitrous areas will allow an almost direct estimation of those intakes at risk of developing deficiency disease. Iodine toxicity is complicated by the fact that some persons are quite tolerant to the element whereas others are highly sensitive to it. There are relatively complete data sets concerning exposure vs. human health effects for both selenium and iodine so that sounder bases probably exist for their dietary recommendations than for many other trace elements.

Selenium is an essential trace element in nutrition for the prevention of disease in humans. Epidemiological studies indicate an association between low nutritional selenium status and increased risks of cardiomyopathy, cardiovascular disease, and carcinogenesis in various sites of the body. The role of selenium supplementation in the prevention and treatment of AIDS-related pathology has been considered. Selenoproteins discovered in mammalian cells may account for the essentiality of selenium in the body's antioxidant defense; thyroid hormone function; immune system function, particularly the cellular immunity; formation of sperm; and functioning of the prostate gland. The seleno-organic compounds, primarily L-(+)-selenomethionine, generally are recognized as safe and effective forms of selenium supplementation. The nutritionally recommended dose of elemental selenium is estimated at 50 to 200 mg per day. There is, however, increased discussion of a pharmacological dose of selenium, significantly higher than the nutritional dose of the microelement, to treat active conditions. One way of increasing the tissue levels of selenium is to combine its ingestible form with a nutrient bioavailability enhancing compound. (87 Refs.)

The role of metals in ischemia/reperfusion injury of the liver.

Arora AS; Gores GJ
Center for Basic Research in Digestive Diseases, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA.
Semin Liver Dis (UNITED STATES) Feb 1996, 16 (1) p31-8

No abstract.

Effect of selenium on 1,2-dimethylhydrazine-induced intestinal cancer in rats.

Jao SW; Shen KL; Lee W; Ho YS
Division of Colon and Rectal Surgery, National Defense Medical Center, Tri-Service General Hospital Taipei, Taiwan, Republic of China.
Dis Colon Rectum (UNITED STATES) Jun 1996, 39 (6) p628-31

PURPOSE: This study was designed to determine the cancer prevention and therapeutic effects of selenium on rats treated with 1,2-dimethylhydrazine (DMH). METHODS: One hundred sixty Spraque-Dawley male rats were divided into seven groups and received 20 mg/kg/week DMH, subcutaneously for 20 weeks. Two different dosages of selenium (8 and 4 ppm) were administered to the rats through drinking water during DMH treatment (B and C groups) or one month before and during DMH treatment (D and E groups). The rats of Groups A (control group), B, C, D, and E were killed immediately after the last DMH injection. The incidence of intestinal cancer in each group was compared. Eight ppm selenium was also administered to rats after DMH treatment (Group F), and survival times were observed and compared with Group G (treated with DMH only). RESULTS: Rats of Groups B and D received 8 ppm selenium and had a significantly decreased incidence of intestinal cancer (from 65.8 percent (Group A) to 33.3 percent (Group B) and 27.8 percent (Group D); P = 0.0225 and 0.0038). Rats receiving 4 ppm selenium had a relatively decreased incidence of intecent (Group A) to 44.4 percent (Group C) and 47.1 percent (Group E) but P > 0.05). Survival time of Groups F and G showed no difference. CONCLUSIONS: Eight ppm selenium provided via drinking water has a significant intestinal cancer prevention effect in the presence of a high dose of DMH (20 mg/kg x 20 weeks), and the cancer therapeutic effect of selenium is doubtful in this animal model.

[Overview--suppression effect of essential trace elements on arteriosclerotic development and it's mechanism]

Saito N
Nippon Rinsho (JAPAN) Jan 1996, 54 (1) p59-66

It is known that the peroxidation of LDL is a trigger for developing arteriosclerosis. The oxidized LDL is produced by either oxidative stress or a few oxidant. Selenium decreased in serum and some organs of stroke-prone spontaneously hypertensive rats (SHRSP), which is a cofactor of glutamine peroxidase. Serum magnesium decreased in patients with diabetes mellitus, with ischemic heart disease, with essential hypertension and with cerebral vascular lesions. Calcium to magnesium ratio was higher in some organs of SHRSP as compared to Wistar Kyoto rats (WKY). These changes accelerated vascular lesions in SHRSP. (21 Refs.)

Selenium in health and disease: a review.

Crit Rev Food Sci Nutr (UNITED STATES) Apr 1997, 37 (3) p211-28

Selenium (Se) was discovered 180 years ago. The toxicological properties of Se in livestock were recognized first; its essential nutritional role for animals was discovered in the 1950s and for humans in 1973. Only one reductive metabolic pathway of Se is well characterized in biological systems, although several naturally occurring inorganic and organic forms of the element exist. The amount of Se available for assimilation by the tissues is dependent on the form and concentration of the element. Se is incorporated into a number of functionally active selenoproteins, including the enzyme glutathione peroxidase, which acts as a cellular protector against free radical oxidative damage and type 1 iodothyronine 5'-deiodinase which interacts with iodine to prevent abnormal hormone metabolism. Se deficiency has been linked with numerous diseases, including endemic cardiomyopathy in Se-deficient regions of China; cancer, muscular dystrophy, malaria, and cardiovascular disease have also been implicated, but evidence for the association is often tenuous. Information on Se levels in foods and dietary intake is limited, and an average requirement for Se in the U.K. has no been established. Available data suggest that intake in the U.K. is adequate for all, except for a few risk groups such as patients on total parenteral nutrition or restrictive diets. (122 Refs.)

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